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Q.6 Clinical Case Scenarios - Complete Answers


Case A - Small Bowel Obstruction (SBO)

Diagnosis: Mechanical small bowel obstruction (SBO) - supported by colicky periumbilical pain, vomiting, obstipation (no stool/flatus x 24h), distension, high-pitched bowel sounds, and plain X-ray showing multiple air-fluid levels with dilated bowel loops.

i) Common Causes of SBO in Adults

The causes are classified as extrinsic, intrinsic, or intraluminal (Maingot's Abdominal Operations, p. 605):
Extrinsic (most common overall):
  • Adhesions - #1 cause in adults (~60-75%); postoperative (most common), postinflammatory, or congenital. This patient's prior episode 2 years ago points to adhesive SBO.
  • Hernias - external (inguinal, femoral), incisional, or internal hernias
  • Volvulus, carcinomatosis, external neoplasm, intra-abdominal abscess
Intrinsic (within bowel wall):
  • Crohn's disease (stricture)
  • Primary intestinal neoplasm (e.g. small bowel tumor)
  • Intestinal tuberculosis
  • Radiation stricture
  • Intussusception
Intraluminal:
  • Gallstone ileus
  • Phytobezoar
  • Foreign body
  • Parasite infestation (e.g. Ascaris)
Most likely in this patient: adhesions (prior episode resolving with conservative management = adhesive SBO recurrence).

ii) Initial Management Steps

A - Airway, B - Breathing, C - Circulation (resuscitation first):
  1. IV Access + Fluid Resuscitation - Insert 2 large-bore IV cannulas; start IV fluids (Normal saline or Ringer's lactate) to correct dehydration. Monitor urine output (target >0.5 mL/kg/hr via urinary catheter).
  2. NGT (Nasogastric Tube) Insertion - Decompress the stomach; relieves vomiting, reduces aspiration risk, and allows monitoring of output.
  3. NPO (Nil Per Oral) - Strict nil by mouth.
  4. Monitoring - Vital signs, urine output, O2 saturation. Pulse oximetry. ECG baseline.
  5. Investigations:
    • Blood: CBC, electrolytes, BUN/creatinine, LFT, serum lactate, coagulation profile, blood group & cross-match
    • ABG if indicated
    • Plain AXR (already done - confirms SBO)
    • CT Abdomen with contrast - gold standard; identifies level, cause, and any strangulation/ischemia
  6. Electrolyte Correction - Correct hyponatremia, hypokalemia (common with vomiting).
  7. Pain Relief - Judicious analgesia (IV opioid if needed); do not withhold.
  8. Antibiotics - Broad-spectrum IV antibiotics if strangulation or perforation suspected.
  9. Conservative (Non-operative) Management for simple partial SBO:
    • Continue IV fluids + NGT decompression ("drip and suck")
    • Reassess every 4-6 hours
    • If no improvement in 24-48 hours or clinical deterioration - proceed to surgery
  10. Surgical Intervention - Indications: complete obstruction, signs of strangulation (peritonism, fever, rising lactate, tachycardia, blood per rectum), closed-loop obstruction, failure of conservative management.
    • Laparotomy or laparoscopy: adhesiolysis, bowel resection if non-viable bowel.

iii) Complications if Not Treated in Time

ComplicationMechanism
Intestinal strangulationVascular compromise from mesenteric compression
Bowel ischemia and necrosisProgressive strangulation → transmural infarction
Perforation and peritonitisNecrotic bowel ruptures → generalized peritonitis
Sepsis / Septic shockBacterial translocation, bowel perforation
Hypovolemic shockFluid sequestration in bowel ("third spacing"), vomiting
Electrolyte imbalancesHyponatremia, hypokalemia, metabolic alkalosis
Aspiration pneumoniaFrom persistent vomiting
Acute kidney injuryFrom dehydration and hypoperfusion
DeathUntreated strangulation has very high mortality

Case B - Incisional Hernia

Diagnosis: Incisional hernia through the lower midline laparotomy scar from the hysterectomy 2 years ago.
Classic features: painless midline swelling, increases on coughing/straining (positive cough impulse), reduces on lying down, at the site of a previous midline incision.

i) Most Likely Diagnosis

Incisional (postoperative ventral) hernia - a failure of fascial tissues to heal and close following laparotomy, resulting in herniation of bowel/omentum through the fascial defect, covered by a peritoneal sac (Maingot's Abdominal Operations, p. 167).

ii) Risk Factors

Patient-specific risk factors (Maingot's, p. 168):
CategoryFactors
This patient has:Obesity (BMI), prior laparotomy (hysterectomy), midline incision
General patient factorsAdvanced age, malnutrition, ascites, corticosteroid use, diabetes mellitus, cigarette smoking, obesity
Wound-relatedWound infection (most significant prognostic factor), postoperative sepsis
Technical factorsWound closed under excessive tension, type of suture, incision orientation (midline > transverse), suture technique
Surgery typeEmergency surgery increases risk; midline and transverse incisions have highest incidence
In this patient: obesity is the major identifiable risk factor, combined with a lower midline incision and prior abdominal surgery.

iii) Treatment Options

Treatment of ventral incisional hernia is operative repair (Maingot's, p. 169). Three main approaches:
  1. Primary Suture Repair
    • Direct fascial closure without mesh
    • High recurrence rate (~50%); reserved for small defects (<2 cm)
    • Not recommended for large or recurrent hernias
  2. Open Mesh Repair (with prosthetic mesh)
    • Onlay - mesh placed anterior to fascia
    • Sublay (Rives-Stoppa retromuscular) - mesh placed in retromuscular space (preferred; lowest recurrence)
    • Inlay - mesh bridging the defect (higher recurrence)
    • Significantly reduces recurrence compared to suture repair alone
  3. Laparoscopic Repair (IPOM - Intraperitoneal Onlay Mesh)
    • Minimally invasive
    • Preferred for obese patients (like this patient) - reduced wound complications
    • Uses composite mesh (coated to prevent adhesions to bowel)
    • Shorter hospital stay, less pain, faster recovery
For this obese patient with a lower midline incisional hernia: laparoscopic IPOM repair or open Rives-Stoppa retromuscular mesh repair is recommended.

Case C - Upper GI Bleed / Hematemesis

Diagnosis: Bleeding peptic ulcer (duodenal ulcer most likely)
Features: hematemesis (fresh blood 150 mL), burning epigastric pain between meals (classic duodenal ulcer pattern), NSAID use, smoking, melena (black stool on PR exam), mild epigastric tenderness. No liver disease/alcohol - making varices unlikely.

i) Most Likely Diagnosis

Bleeding duodenal/peptic ulcer - caused by:
  • Chronic NSAID use (inhibits COX-1 → reduces prostaglandins → impairs mucosal protection)
  • Smoking (impairs mucosal blood flow and healing)
  • H. pylori infection (likely underlying; not yet tested)
The pain between meals, absence of alcohol/liver disease, and NSAID use all strongly point to peptic ulcer disease as the source.

ii) Differential Diagnoses

DiagnosisSupporting Features
Duodenal ulcer bleedingMost likely (NSAID use, pain between meals, melena)
Gastric ulcerEpigastric pain, NSAID use
Mallory-Weiss tearPost-vomiting bleed - but this was first episode before vomiting started
Gastric erosions/gastritisNSAID use, alcohol (though denied)
Esophageal varicesNo liver disease, no alcohol - unlikely
Dieulafoy lesionSudden large bleed, no prior symptoms
Esophagitis / reflux esophagitisBurning discomfort, though GERD not primary here
Gastric carcinomaLess likely at 48y, but must exclude on endoscopy
Aortoenteric fistulaPrior aortic surgery - no history here

iii) Initial Management of Hematemesis (UGI Bleed)

Based on Sleisenger & Fordtran's GI and Liver Disease, p. 297:
Step 1 - Resuscitation (ABC priority)
  • Secure 2 large-bore IV cannulas (16G or larger)
  • IV fluid resuscitation: Normal saline or Ringer's lactate
  • Blood transfusion if Hb <7 g/dL or hemodynamically unstable (target Hb 7-9 g/dL)
  • Supplemental oxygen; airway protection (consider intubation if massive bleed or altered consciousness)
  • Urinary catheter to monitor urine output
Step 2 - Assessment & Monitoring
  • Vital signs monitoring (HR, BP, SpO2)
  • NG tube placement - aspirate gastric contents; assess for active bleeding
  • Blood tests: CBC, coagulation (PT/INR, APTT), LFT, U&E, blood group & cross-match (hold 4-6 units blood)
  • Assess severity using Rockall Score (pre-endoscopy) or Glasgow-Blatchford Score to guide admission and urgency
Step 3 - NPO + Stop Aggravating Drugs
  • Nil per oral
  • Stop NSAIDs immediately
Step 4 - Pharmacological Treatment
  • IV Proton Pump Inhibitor (PPI): IV Pantoprazole or Omeprazole 80 mg bolus, then 8 mg/hr infusion (reduces rebleeding by raising gastric pH >6, stabilizing clot)
  • IV Somatostatin analogue (Octreotide): if variceal bleed suspected
  • Antibiotics: if cirrhosis or variceal bleed
Step 5 - Urgent Upper GI Endoscopy (OGD)
  • Within 24 hours for stable patients; within 12 hours for high-risk patients
  • Confirms diagnosis (peptic ulcer, site of bleed)
  • Provides endoscopic hemostasis:
    • Adrenaline injection (epinephrine 1:10,000)
    • Heater probe thermocoagulation / bipolar electrocoagulation
    • Hemoclip application
    • Combination therapy (injection + thermal/mechanical) preferred
Step 6 - Post-Endoscopy Care
  • Continue high-dose IV PPI for 72 hours, then oral PPI
  • H. pylori testing (CLO test / biopsy at endoscopy) → eradicate if positive (triple therapy: PPI + Clarithromycin + Amoxicillin for 14 days)
  • Recheck Hb at 4-6 hours
Step 7 - Surgery (if endoscopy fails)
  • Indications: persistent or recurrent bleeding despite 2 endoscopic attempts, hemodynamic instability
  • Procedures: oversewing of the bleeding vessel (ulcer), partial gastrectomy
  • Alternatively: Interventional radiology (IR) angioembolization in high surgical risk patients

References:
  • Maingot's Abdominal Operations, Table 29-1 (Causes of Mechanical Bowel Obstruction) and pp. 167-169 (Incisional Hernia)
  • Sleisenger & Fordtran's Gastrointestinal and Liver Disease, pp. 283-297 (Upper GI Bleeding)
  • Schwartz's Principles of Surgery, 11th Edition (Pathophysiology of SBO)
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